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Isolated hypocortisolism due to ACTH deficiency is a rare condition that can be caused by homozygous or compound heterozygous mutations in the gene encoding proopiomelanocortin (POMC). Loss of function mutations of POMC gene typically results in adrenal insufficiency, obesity and red hair. We
Sequential cleavage of the precursor protein pre-pro-opiomelanocortin (POMC) generates the melanocortin peptides adrenocorticotrophin (ACTH), melanocyte-stimulating hormones (MSH) alpha, beta and gamma as well as the opioid-receptor ligand beta-endorphin. While a few cases of isolated ACTH
A 62-year-old Asian British female presented with increasing tiredness. She had multiple co-morbidities and was prescribed steroid inhalers for asthma. She had also received short courses of oral prednisolone for acute asthma exacerbations in the last 2 years. Unfortunately, the Lately, it has been revealed that cortisol (hydrocortisone) secretion is lower than previously thought. Replacement doses of 10-15 mg/24 h seem sufficient in non-obese individuals. The day-night variation and in particular the fast oscillations in plasma cortisol concentration may be important for
Prader-Willi syndrome (PW) is a rare genetic disorder with multi-organ system involvement. These patients present many perioperative challenges including sleep-related breathing disorders, morbid obesity, thick salivary secretions, mental retardation, and difficult intravenous access. PW has been
The adverse effects of corticosteroids are well-known and occur more frequently when corticosteroids are used perorally or intravenously. The management of uveitis, which normally consists of topical corticosteroids and mydriates, can be challenging. We report a case in which continuous use of
Primary adrenal insufficiency (Addison's disease, AD) requires lifelong steroid substitution. Excess exogenous glucocorticoids promote abdominal obesity, insulin-glucose imbalance, and hypertension. Reliable markers of the adequate glucocorticoid replacement are lacking. Visfatin is a
Congenital adrenal insufficiency is caused by specific genetic mutations. Early suspicion and definite diagnosis are crucial because the disease can precipitate a life-threatening hypovolemic shock without prompt treatment. This study was designed to understand the clinical manifestations including
Objectives: Potent glucocorticoids (GC) cause iatrogenic Cushing Syndrome (ICS) due to suppression of hypothalamo-hypophyseal-adrenal (HPA) axis and later even adrenal insufficiency (AI). The aim of this study is to review the clinical
BACKGROUND
Obesity and asthma have become increasingly prevalent conditions in recent years; they often coexist and place a significant burden on the National Health Service. Asthma in the obese is more difficult to treat than in those with a normal body mass index (BMI) and is associated with
The cloning of five rodent obesity genes has constituted a major advance in our understanding of body weight homeostasis. Breakthroughs in human molecular genetics have identified mutations disrupting either rodent homologue/analogue genes or genes involved in the same pathways in obese patients.
OBJECTIVE
Obesity with abdominal body fat distribution (A-BFD) and hypothalamic-pituitary-adrenal (HPA) axis activity are somehow linked, but the exact interactions still need clarification. Obese subjects display normal circulating plasma cortisol concentrations with normal circadian rhythms.
BACKGROUND
Obesity resulting from damage to the hypothalamus, i.e. hypothalamic obesity, is a severe condition that currently lacks any effective evidence-based therapy.
OBJECTIVE
Our goal was to describe the course of hypothalamic obesity in a craniopharyngioma patient treated with distal gastric
We have previously shown that following adrenalectomy, gold thioglucose (GTG)-treated hyperphagic obese mice exhibit anorexia, weight loss and a pronounced hypoglycemia which leads ultimately to their death. In the present study, we sought to determine whether the increased adipose tissue mass which
The effects of adrenalectomy on food intake, weight gain, plasma glucose, and corticosterone levels were investigated in normal untreated controls and gold thioglucose-(GTG) treated hyperphagic obese mice. Adrenalectomy of normal untreated mice was followed by a transient reduction in food intake